Gastrointestinal symptoms are common in diabetes, possibly more than in the general population (Table 23.1). However, there is an imprecise relationship between the symptoms and either demonstrable motor dysfunction (e.g. gastric emptying time) or autonomic neuropathy. Among the additional factors that influence symptoms are hyperglycemia (which increases the perception of visceral sensation, such as gut fullness); and drugs such as metformin, acarbose and incretins (exenatide and liraglutide), which can cause diarrhea and fecal incontinence. There is also a link with psychological stress and psychiatric symptoms of anxiety and depression which doubled the prevalence of GI symptoms in one cross-sectional study. It is important to exclude other endocrine disease which can cause altered gastrointestinal function such as hyper- and hypothyroidism.
Oesophageal transit is delayed in about 30%–50% of subjects with diabetes (mostly because of impaired peristalsis) and is associated with dysphagia, heartburn and chest pain (Figure 23.4). Endoscopy is required to exclude other disorders, such as carcinoma and candidiasis. Minimal symptoms do not require treatment; indeed, no treatment, including prokinetic drugs, has yet been shown to be effective for more severe symptoms attributable to hypomotility. Consider discontinuation of drugs such as calcium channel blockers, which can worsen heartburn. Reflux oesophagitis is also exacerbated by obesity.
Delayed gastric emptying (gastroparesis) of a modest extent occurs in up to 50% of people with diabetes of long standing. Symptoms of gastroparesis are characteristically worse postprandially, include nausea, vomiting, abdominal discomfort and/or fullness and anorexia, and are reported in 5%–12% of all patients with diabetes. Symptoms are often stable for up to 12 years and do not appear to be associated with mortality. They tend to be worse with solids rather than liquids. The pathophysiology is a combination of vagal neuropathy and increased gastrointestinal hormone levels such as glucagon. There is often a history of longstanding poor glycemic control.
Examination can reveal epigastric distension and a succussion splash an hour or two after a liquid meal if the stomach is grossly dilated. Radioisotope scintigraphy is the gold standard method for measuring gastric emptying. Ideally, this should be performed during normoglycemia and with a dual isotope assessment of both solid and liquid emptying. The drawbacks of this test are its expense and significant radiation exposure. A carbon 13 breath test has acceptable specificity and sensitivity and much less radiation.
Diagnosis is often based upon the patient history, in the context of other diabetic complications, especially autonomic neuropathy, and investigations should be carried out to rule out other conditions. Of these oesophagogastroduodenoscopy (OGD) is the most helpful. It is important to remember that some drugs can delay gastric emptying and should be avoided (Box 23.1).
Treatment of symptomatic gastroparesis is difficult; it involves improving glycemic control, eating small meals often (reducing solid components) and administration of prokinetic drugs such as domperidone, metoclopramide and erythromycin (possibly better given intravenously for acute episodes because of tolerance). Severely affected patients may need admission to hospital for intravenous fluids, control of diabetes and possible nasogastric feeding. Placement of a feeding jejunostomy (PEJ) tube to maintain nutrition may be required, but surgical drainage and bypass should be avoided. There have been trials of gastric electrical stimulation via an implanted pacemaker but the results are inconclusive and more studies are required. Because many of these patients may have diabetic nephropathy and a diminished GFR, care must be taken with doses of drugs in order to avoid side effects.
Autonomic neuropathy and sometimes colonization of the hypomotile small bowel by colonic bacteria contribute to ‘diabetic diarrhea,’ but other factors probably play a role. Classically, the diarrhea is intermittent and worse at night. Bouts that last several days may be followed by remissions. The diagnosis is by exclusion, and other possible causes of diarrhea, such as drugs (metformin, acarbose, antibiotics and alcohol), chronic pancreatic insufficiency with malabsorption, and coeliac disease must be considered.
Treatment of diabetic diarrhea is by opioid derivatives (e.g. loperamide) or a broad-spectrum antibiotic if bacterial overgrowth is suspected or proven by hydrogen breath test. Troublesome diarrhea, especially when watery, may respond to the α adrenergic agonists clonidine or limidine (unlicensed indication). The long-acting somatostatin analogue octreotide may be helpful when other measures have failed (Table 23.3).
Constipation is also common in patients with diabetes and autonomic neuropathy and poor glycemic control, though it is usually mild. A thorough history should be taken, including that of drug intake (many narcotics, antihypertensives and antidepressants can cause constipation). Thyroid function and serum calcium and potassium levels should be assessed to exclude metabolic disorders. Other serious pathology, such as colonic carcinoma, must be excluded. If constipation requires treatment, fiber and bulking agents are the first choice, and stimulant laxatives (e.g. senna), osmotic laxatives (e.g. lactulose) or prokinetic drugs are also usually effective.
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Rudy Bilous MD, FRCP, Professor of Clinical Medicine, Newcastle University, Honorary Consultant Endocrinologist, South Tees Foundation Trust, Middlesbrough, UK Richard Donnelly MD, PHD, FRCP, FRACP, Head, School of Graduate Entry Medicine and Health, University of Nottingham, Honorary Consultant Physician, Derby Hospitals NHS Foundation Trust, Derby, UK
A John Wiley & Sons, Ltd., Publication This edition first published 2010, © 2010 by Rudy Bilous and Richard Donnelly. Previous editions: 1992, 1999, 2004
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